Chemokines mediate a range of proinflammatory effects on cells (e.g., leukocytes), such as chemotaxis, degranulation, and integrin activation (Baggiolini et al., Adv. Immunol., 1994;55:97-179; Oppenheim et al., Annu. Rev. Immunol., 1991;9:617-648; Miller et al., Crit. Rev. Immunol., 1992;12:17-46). These effects are mediated by binding to the seven-transmembrane-spanning G-protein coupled receptors (Baggiolini et al., Adv. Immunol., 1994;55:97-179; Murphy, Annu. Rev. Immunol., 1994;12:593-633; Schall et al., Curr. Opin. Immunol., 1994;6:865-873; Gerard et al., Curr. Opin. Immunol., 1994;6;140-145; Mackay, Curr. Bio., In press). Chemokine receptors also serve as coreceptors for Human Immunodeficiency Virus (HIV) entry into cells. This came from observations that RANTES, MIP-1α, and MIP-1β suppressed infection of susceptible cells in vitro by macrophage-tropic primary HIV-1 isolates (Cocchi et al., Science (Wash. D.C.), 1995;270:1811-1815). The chemokine receptor CXCR-4 was found to support infection and cell fusion of CD4+ cells by laboratory-adapted, T-tropic HIV-1 strains (Feng et al., Science (Wash. D.C.), 1996;272:872-877). CCR-5, which is a RANTES, MIP-1α, and MIP1β receptor, was subsequently identified as the principal coreceptor for primary macrophage-tropic strains (Choe et al., Cell, 1996;85:1135-1148; Alkhatib et al., Science (Wash. D.C.), 1996;272:1955-1958; Doranz et al., Cell, 1996;85:1149-1158; Deng et al., Nature (Lond.) 1996;381:661-666; Dragic et al., Nature (Lond.), 1996;381:667-673). The importance of CCR-5 for HIV-1 transmission was underscored by the observation that certain individuals who had been repeatedly exposed to HIV-1 but remained uninfected had a defect in CCR-5 expression (Liu et al., Cell, 1996; 86:367-377; Samson et al., Nature (Lond.), 1996;382:722-725; Dean et al., Science (Wash. D.C.), 1996;273:1856-1862; Huang et al., Nature Med., 1996;2:1240-1243). These noninfectable individuals were found to be homozygous for a defective CCR-5 allele that contains an internal 32-base pair deletion (CCR-5 Δ32). The truncated protein encoded by this gene is apparently not expressed at the cell surface. CCR-5 Δ32 homozygous individuals comprise ˜1% of the Caucasian population and heterozygous individuals comprise ˜20%. In studies of about 2700 HIV-1 infected individuals, no Δ32 homozygotes were found. Individuals who are heterozygous for Δ32 CCR-5 allele have been shown to progress more slowly to AIDS than wild-type homozygous individuals (Samson et al., Nature (Lond.), 1996;382:722-725; Dean et al., Science (Wash. D.C.), 1996;273:1856-1862; Huang et al., Nature Med., 1996;2:1240-1243). Thus, the identity of CCR-5 as the principal coreceptor for primary HIV isolates provides an opportunity to understand pathogenesis HIV infection and to identify new avenues for the treatment of HIV (e.g., HIV-1) infection. Prior studies of CCR5 also provide a basis for further studies into the pathogenesis of inflammatory diseases and for developing novel treatments for inflammatory diseases.